Determining the hydroxylation status of NAA10-Trp38

NAA10 is the major human N-terminal acetyltransferase (NAT). The KAT activity of NAA10 towards hypoxia-inducible factor 1α (HIF-1α) was recently reported to depend on the hydroxylation at Trp38 of NAA10 by factor inhibiting HIF-1α (FIH). As a consequence, Trp38 hydroxylation status was proposed to act as a general NAA10-switch between its NAT and KAT state. We attempted to quantify the degree of hydroxylation of NAA10. We could not detect any hydroxylation of Trp38 of NAA10 in several human cell lines.